Lactate utilization and production were investigated in perfused lungs under aerobic conditions. The perfused lung incorporated labelled lactate with 44% of the total tissue radioactivity appearing in the TCA-soluble fraction, 15% in lipids and 15% in lung protein, and 24% oxidized to C14O2. Hydrolysis of phospholipids (PL) resulted in over 84% of PL radioactivity appearing in phospholipid fatty acids (PLFA) with the remainder distributed equally in the nonsaponifiable and phospholipid glycerol fractions. Lactate utilization showed a 15 fold increase when circulating levels of lactate were raised from 0.4 to 11mM. In a separate experiment, glucose incorporation into lung lipids, nucleic acids and proteins as well as oxidation to CO2 were significantly (P less than 0.05) depressed with elevated levels of circulating lactate (6mM). Lipogenesis from glucose was proportionally more depressed in PL than neutral lipids with a 64% decrease in incorporation of glucose into PLFA. Rate of lactate production in the perfused lung was not altered when circulating levels of lactate were raised from 0.4mM to 6mM. These data indicate that the lung can produce and utilize lactate simultaneously and that lactate serves as a potential substrate for the lung.